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首页> 外文OA文献 >Hypoxia-Inducible Erythropoietin Signaling in Squamous Dysplasia and Squamous Cell Carcinoma of the Uterine Cervix and Its Potential Role in Cervical Carcinogenesis and Tumor Progression
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Hypoxia-Inducible Erythropoietin Signaling in Squamous Dysplasia and Squamous Cell Carcinoma of the Uterine Cervix and Its Potential Role in Cervical Carcinogenesis and Tumor Progression

机译：缺氧诱导的促红细胞生成素信号传导在子宫颈鳞状增生和鳞状细胞癌中的作用及其在宫颈癌变和肿瘤进展中的潜在作用

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Tissue hypoxia is a characteristic property of cervical cancers that makes tumors resistant to chemo- and radiation therapy. Erythropoietin (Epo) is a hypoxia-inducible stimulator of erythropoiesis. Acting via its receptor (EpoR), Epo up-regulates bcl-2 and inhibits apoptosis of erythroid cells and rescues neurons from hypoxic damage. In addition to human papillomavirus infection, increased bcl-2 expression and decreased apoptosis are thought to play a role in the progression of cervical neoplasia. Using reverse transcriptase-polymerase chain reaction and Western blotting we showed that HeLa and SiHa cervical carcinoma cells and human cervical carcinomas express EpoR, and that hypoxia enhances EpoR expression. Exogenous Epo stimulated tyrosine phosphorylation and inhibited the cytotoxic effect of cisplatin in HeLa cervical carcinoma cells. Using immunohistochemistry, we examined the expression of Epo, EpoR, p16, hypoxia-inducible factor (HIF)-1α, and bcl-2 in benign and dysplastic cervical squamous epithelia and invasive squamous cell carcinomas (ISCCs). EpoR expression in benign epithelia was confined to the basal cell layers, whereas in dysplasias it increasingly appeared in more superficial cell layers and showed a significant correlation with severity of dysplasia. Diffuse EpoR expression was found in all ISCCs. Expression of Epo and HIF-1α was increased in dysplasias compared to benign epithelia. Focal Epo and HIF-1α expression was seen near necrotic areas in ISCCs, and showed correlation in their spatial distribution. Significant correlation was found between expression of EpoR, and p16 and bcl-2 in benign and dysplastic squamous epithelia. Our results suggest that increased expression of Epo and EpoR may play a significant role in cervical carcinogenesis and tumor progression. Hypoxia-inducible Epo signaling may play a significant role in the aggressive behavior and treatment resistance of hypoxic cervical cancers.
机译：组织缺氧是宫颈癌的特征，它使肿瘤对化学疗法和放射疗法产生抵抗力。促红细胞生成素（Epo）是一种可诱导低氧的促红细胞生成素。 Epo通过其受体（EpoR）起作用，上调bcl-2并抑制红系细胞凋亡，并使神经元免受缺氧损伤。除了感染人乳头瘤病毒外，bcl-2表达的增加和凋亡的减少也被认为在宫颈癌的发展中起着重要作用。使用逆转录酶-聚合酶链反应和蛋白质印迹，我们表明HeLa和SiHa宫颈癌细胞和人宫颈癌表达EpoR，而缺氧增强EpoR的表达。外源性Epo刺激酪氨酸磷酸化并抑制顺铂对HeLa宫颈癌细胞的杀伤作用。使用免疫组织化学，我们检查了Epo，EpoR，p16，缺氧诱导因子（HIF）-1α和bcl-2在良性和发育异常的宫颈鳞状上皮细胞和浸润性鳞状细胞癌（ISCC）中的表达。 EpoR在良性上皮细胞中的表达仅限于基底细胞层，而在不典型增生中，EpoR越来越多地出现在较浅的细胞层中，并且与不典型增生的严重程度密切相关。在所有ISCC中均发现了弥漫性EpoR表达。与良性上皮细胞相比，异型增生中Epo和HIF-1α的表达增加。在ISCC的坏死区域附近可见到灶性Epo和HIF-1α表达，并且在它们的空间分布中显示出相关性。在良性和异常增生的鳞状上皮细胞中，EpoR的表达与p16和bcl-2的表达之间存在显着相关性。我们的结果表明，Epo和EpoR的表达增加可能在宫颈癌变和肿瘤进展中起重要作用。低氧诱导的Epo信号传导可能在低氧子宫颈癌的侵袭行为和治疗抵抗中起重要作用。

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